Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Indigo Carmine ; Indoles ; therapeutic use ; Leukemia, Promyelocytic, Acute ; drug therapy ; Male ; Recurrence

Objective To summarize the clinical features and vascular lesions in patients who suffered from cerebellar infarction with vertebral artery hypoplasia(VAH). Methods Retrospective analysis was used in the research. The selected patients suffered from cerebellar infarction with VAH or stenosis (stenosis rate≥50%). Seventy-one patients with cerebellar infarction were enrolled. There were 34 patients in VAH group and 37 patients in vertebral artery stenosis group. The age, sex, risk factors, clinical manifestations and characteristics of vascular examination were compared. Results The age, sex, risk factors between two groups had no significant differences (P>0.05). The scores of National Institutes of Health Stroke Scale (NIHSS) between two groups had no significant difference (P>0.05). The proportion of early neurological deterioration in VAH group (41.2%, 14/34) was higher than that in vertebral artery stenosis group (18.9%, 7/37), χ2=4.21, P<0.05. There were more patients with anterior circulation artery stenosis in the VAH group (35.3%, 12/34), compared with that in artery stenosis group (13.5%, 5/37),χ2=4.62, P<0.05. Except the ipsilateral vertebral artery, other arteries stenosis in VAH group (44.1%, 15/34) was significantly higher than that in vertebral artery stenosis group (13.5%, 5/37),χ2=8.20, P<0.05. Conclusions Cerebellar infarction with vertebral artery hypoplasia is more likely to have multiple cerebral arterial stenosis (stenosis rate ≥50%). The patients who suffered from cerebellar infarction with vertebral artery hypoplasia might be prone to early neurological deterioration.

Objective To investigate the mechanism by which rosiglitazone affects no-reflow following reperfusion after acute myocardial infarction(AMI).Methods Forty-five SD rats were randomly divided into sham-operated group,normal saline treated group and rosiglitazone treated group(at dose of 3 mg?kg-1?d-1,for 14 d),15 rats in each group.To establish no-reflow model,the rats of the latter two groups received coronary artery ligation for 3 h and reopening for 2 h.Then pathological staining for no-reflow area,chemical assay for MPO activity,immunohistochemistry and RT-PCR for protein and mRNA expressions of ICAM-1 and P-selectin in myocardium were performed.Results No-reflow area in rosiglitazone treated group was significantly reduced,compared with that in normal saline treated group(P

0.05).Compared with those in Sham group,LVWI,the typeⅠCVF,type Ⅲ CVF andⅠ/Ⅲ ratio in NIZ were increased significantly in MI group.Compared with those in MI group,the LVWI,the type ⅠCVF,type Ⅲ CVF andⅠ/Ⅲ ratio in NIZ were decreased significantly in Sim groups(but higher than those in Sham group).Compared with MI groups,left ventricular function in rats treated with simvastatin was also obviously improved.(2) Contrasted to those in MI group,the expressions of TGF-?1 and Smad3 were down-regulated in simvastatin treatment groups(but higher than those in Sham group).Conclusions Sim can ameliorate ventricular remodeling and ventricular function in rats induced by MI,and the mechanisms can be independent of its lipid-lowering and associated with inhibition of TGF-?1/Smad3 signal transduction.

Objective To investigate the beneficial effects of simvastatin on ventricular remodeling in rats after myocardial infarction and the possible mechanisms involved.Methods The myocardial infarction rat model was reproduced.Twenty-four hours after infarction,the survived rats were randomly divided into myocardial infarction group(MI group,n=9),simvastatin 10mg group [10mg/(kg?d),Sim1 group;n=8],simvastatin 20mg group [20mg/(kg?d),Sim2 group;n=10] and simvastatin 40mg group [40mg/(kg?d),Sim4 group;n=9].A sham-operated group(Sham group;n=10) served as control.Four weeks later,the serum lipid level,hemodynamic indexes and left ventricular weight index(LVWI) were measured.The changes in rats' myocardial tissue were observed with HE staining;the cross-sectional area of myocardial cells was calculated.The expressions of transforming growth factor ?1(TGF-?1) and TGF-?-activated kinase 1(TAK1) in non-infarction area were determined by Western blotting and reverse transcription polymerase chain reaction(RT-PCR).Results The hemodynamic indexes,LVWI,cross-sectional area of myocardial cells and the pathological changes were improved,and mRNA and protein expressions of TGF-?1 and TAK1 were down-regulated significantly in the 3 Sim-treated groups compared with that in MI group.The indices mentioned above were significantly different in Sim2 and Sim4 group compared with Sim4 group(P0.05).Conclusion The inhibitory effect of simvastatin on ventricular remodeling after acute myocardial infarction is independent of its lipid-regulating effect,but possibly attributed to its action in inhibiting the TGF-?1/AK1 signal transduction.Within the concentration of 20mg/(kg?d),the therapeutic efficacy of simvastatin may be more obvious with an increase in its dosage.

Background Eicosapentaenoic acid(EPA)function as the critical lipid mediators involved in several biological events in human body and play important role in suppressing the genesis of vascular endothelial growth factor (VEGF),migration and proliferation of vascular endothelial cells.Many ocular diseases were proved to be associated with neovascularization.Objecfive The purpose of this study was to investigate the inhibitory effect of EPA on the proliferation of human umbilical vein endothelial cells (HUVEC) indueed by VEGF. Methods HUVEC strain was cultured and passaged,and difierent concentrations of EPA were added to the medium with and without VEGF.The cultured cells were identified by antiofactor Ⅷ polyclonal antibody.The suppressing role of different concentrations of EPA on the proliferation of VEGF-induced or-uninduced HUVEC was assessed by MTT method.The influence of difierent concentrations of EPA on the cellular cycle of VEGF-induced HUVEC was assayed using flow eytometry.The expression of Flk-1,a receptor of VEGF,in the HUVEC Was detected by immunohistochemistry. Results Cultured HUVEC showed the ftlsiform in shape and presented with the cobblestone-like arrangement with the positive response for Ⅷ factor-related antigen.Various concentrations of EPA showed obviously inhibitory effect on VEGF-induced or-unindueed HUVEC at a dose-dependent manner (F=23.072.P=0.000).The inhibitory ability of EPA on VEGF-induced HUVEC was stronger than VEGF-uninduced HUVEC(F=41.417,P=0.000).In 24,48 and 72 hours,the action of EPA on the proliferation of HUVEC was gradually enhanced with the prolong of time(F=1.495,P=0.236).Cell cycle analysis indicated that EPA arrested VEGF-induced HUVEC in G0/G1 phase.The ratio of HUVEC in G0/G1 phase in EPA group was(75.83±1.56)%,and that in control groups was(68.62±1.44)%,showing a significant difference between them(t=-5.88,P=0.00),and no apoptosis of HUVEC was found in both groups.Flk-1 was strongly expressed in the cellular nucleus and cytoplasm in control group.However,the positive expressing intensity of Flk-1 in the HUVEC weakened,and the positive cell number was evidently less in EPA group. Conclusion EPA can inhibit the proliferation of VEGF induced HUVEC through arresting the synthesis of DNA of HUVEC and downregulate the expression of Flk-1 in HUVEC.These results suggest that EPA might exert an antiangiogenic effect.

Objective To explore the diagnosis and TNM stage effect of serum CYFRA21-1,VEGF and PDGF in patients with non-small cell lung cancer.Methods The electrochemiluminescence immunoas- say was used to detect serum CYFRA21-1,and the sandwich enzyme-linked immunoabsorbentassay(ELISA) was used to detect serum VEGF and PDGF in patients with non-small cell lung cancer and 30 normal healthy controls.Results Compared with healthy control group,the level of serum CYFRA21-1,VEGF and PDGF in non-small cell lung cancer group were much higher(P0.05).The serum CYFRA21-1 level was positively correlated with VEGF and PDGF(P

1H NMR metabonomics approach was used to reveal the chemical difference of urine between patients with Xiao-Chaihu Tang syndrome (XCHTS) and healthy participants (HP). The partial least square method was used to establish a model to distinguish the patients with Xiao-Chaihu-Tang syndrome from the healthy controls. Thirty-four endogenous metabolites were identified in the 1H NMR spectrum, and orthogonal partial least squares discriminant analysis showed the urine of patients with Xiao-Chaihu Tang syndrome and healthy participants could be separated clearly. It is indicated that the metabolic profiling of patients with Xiao-Chaihu Tang syndrome was changed obviously. Fifteen metabolites were found by S-pot of OPLS-DA and VIP value. The contents of leucine, formic acid, glycine, hippuric acid and uracil increased in the urine of patients, while threonine, 2-hydroxyisobutyrate, acetamide, 2-oxoglutarate, citric acid, dimethylamine, malonic acid, betaine, trimethylamine oxide, phenylacetyl glycine, and uridine decreased. These metabolites involve the intestinal microbial balance, energy metabolism and amino acid metabolism pathways, which is related with the major symptom of Xiao-Chaihu Tang syndrome. The patients with Xiao-Chaihu Tang syndrome could be identified and predicted correctly using the established partial least squares model. This study could be served as the basis for the accurate diagnostic and reasonable administration of Xiao-Chaihu-Tang syndrome.
Humans ; Least-Squares Analysis ; Medicine, Chinese Traditional ; Metabolome ; Metabolomics ; Proton Magnetic Resonance Spectroscopy ; Syndrome ; Urinalysis

OBJECTIVETo observe the effects of Ganoderma lucidum spores on Cytochrome C (Cyt-C) and mitochondrial calcium in the testis of NIDDM rats.

METHODSFifty male Wistar rats were divided randomly into three groups: model, ganoderma and normal control, the first two groups injected with 2% STZ through vena caudalis, and the last one with half-and-half sodium citrate/citrate buffer solution. Two weeks after normal diet, glucose tolerance tests were performed and the rats with abnormal glucose tolerance from the model and ganoderma groups received high-fat and high-carbohydrate food, the ganoderma group given Ganoderma lucidum spores (250mg/[ kg x d] ) in addition, both for 10 weeks. Glucose tolerance tests were repeated 1 day before the end of the experiment and the rats were castrated and relevant indexes measured.

RESULTSThe NIDDM model was successfully constructed. In the model group, the levels of mitochondrial Cyt-C and mitochondrial calcium were significantly lower (P <0. 05) while that of the plasma Cyt-C was significantly higher than in the ganoderma and the control groups.

CONCLUSIONCyt-C and calcium ion are involved in the damage of the testis. Ganoderma lucidum spores can protect the testis of NIDDM rats.

Animals ; Calcium ; metabolism ; Cytochromes c ; metabolism ; Diabetes Mellitus, Experimental ; drug therapy ; Diabetes Mellitus, Type 2 ; drug therapy ; Male ; Mitochondria ; drug effects ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Reishi ; Testis ; drug effects ; metabolism

OBJECTIVETo study the inhibitory effect of paeoniflorin (PAE) on TNF-α-induced TNF receptor type I (TNFR1)-mediated signaling pathway in mouse renal arterial endothelial cells (AECs) and to explore its underlying molecular mechanisms.

METHODSMouse AECs were cultured in vitro and then they were treated by different concentrations PAE or TNF-α for various time periods. Expression levels of intercellular cell adhesion molecule-1 (ICAM-1) were detected in the normal group (cultured by serum-free culture media), the TNF-α group (cultured by 2-h serum-free culture media plus 6-h TNF-α 30 ng/mL), the low dose PAE group (cultured by 2-h PAE 0.8 μmo/L plus 6-h TNF-α 30 ng/mL), the middle dose PAE group (cultured by 2-h PAE 8 μmol/L plus 6-h TNF-α 30 ng/mL), the high dose PAE group (cultured by 2-h PAE 80 μmol/L plus 6-h TNF-α 30 ng/mL) with Western blot analysis. Nuclear translocation of transcription factor NF-κB (NE-κB) was detected in the normal group (cultured by serum-free culture media), the TNF-α group (cultured by 2-h serum-free culture media plus 45-mm TNF-α 30 ng/mL), and the high dose PAE group (cultured by 2-h PAE 80 μmol/L plus 45-min TNF-α 30 ng/mL) by immunofluorescent staining. Expression levels of the phosphorylation of extracellular signal-regulated (protein) kinase (ph-ERK) and p38 (ph- p38) were detected in the normal group (cultured by serum-free culture media) and the high dose PAE group (2-h PAE 80 μmol/L culture) by Western blot. NF-κB inhibitor-α (IκBα) protein expressions were detected in the normal group (cultured by serum-free culture media), the TNF-α group (cultured by 2-h serum-free culture media plus 30-min TNF-α 30 ng/mL), the high dose PAE group (cultured by 2-h PAE 80 μmol/L plus 30-min TNF-α 30 ng/mL), the p38 inhibitor group (SB group, pretreatment with SB238025 25 μmol/L for 30 min, then treated by PAE 80 μmol/L for 2 h, and finally treated by TNF-α 30 ng/mL for 30 min), the ERK inhibitor group (PD group, treated by PD98059 50 μmol/L for 30 min, then treated by PAE 80 μmol/L for 2 h, and finally treated by TNF-α 30 ng/mL for 30 min) by Western blot.

RESULTSCompared with the normal group, ICAM-1 protein expression levels obviously increased (P < 0.01). Compared with the TNFα group, ICAM-1 protein expression levels were obviously inhibited in the high dose PAE group (P < 0.05). Protein expression levels of ph-p38 and ph-ERK were obviously higher in the hIgh dose PAE group (P < 0.05). Compared with the normal group, IκBα protein expression levels obviously decreased in the TNF-α group (P < 0.01). Compared with the TNFα group, TNF-α-induced IκBα degradation could be significantly inhibited in the high dose PAE group (P < 0.01); the inhibition of PAE on IκBα degradation could be significantly inhibited in the SB group (P < 0.05). NF-κB/p65 signal was mainly located in cytoplasm in the normal group. NF-κB/p65 was translocated from cytoplasm to nucleus after stimulated by 45 min TNF-α in the TNF-α group, while it could be significantly inhibited in the high dose PAE group.

CONCLUSIONSPAE inhibited TNF-α-induced expression of lCAM-1. Its action might be associated with inhibiting TNFR1/NF-κB signaling pathway. p38 participated and mediated these actions.

Animals ; Cells, Cultured ; Endothelial Cells ; cytology ; drug effects ; Glucosides ; pharmacology ; Intercellular Adhesion Molecule-1 ; metabolism ; Mice ; Monoterpenes ; pharmacology ; NF-kappa B ; metabolism ; Receptors, Tumor Necrosis Factor ; metabolism ; Signal Transduction ; drug effects ; Tumor Necrosis Factor-alpha ; pharmacology